/

§
.
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Urology

-- ·,
. Lecture r DOne By Page
1 Acronyms --- 1
2 Urological presentation & investigation --- 3
3 Urinary TB --- 21
4 Urodynamic studies --- 29
5 Pediatric urology --- 34
6 Urinary incontinence --- 51
7 Stones
8 Prostate CA
9 Neurogenic bladder
10 Renal tumors
11 Urinary retention
12 Double J. Stents
13 Foley's Catheter
14 KUB & CT 63
15
. Urinary tract obstruction
o.JL...

16 Notes
17 ED
18 Trauma
19 Benign prostatic hyperplasia
20 Testicular CA
21 Bladder CA
22 Urethral CA
23 UTI _,.J14..iJ"
(.5"'-" , .) 121
24 Infertility Jly:. .J...)AC 125
25 Renal transplantation 129
26 Benign scrotal swelling 133
27 OSCE +Notes --- 137

pediatric urology t_,...o_,.. t) 6 2 u.- •

<,>.JL......:JI Ui4-o) .:.l!L:.) w.;c. u.- 22 7 u.- •
renal trauma , testicular cancer o
201512014 t} 26 u-1) 23 t.).o •
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• 'Dx.
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• PCNL pe.r cutaneou.A
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e Ttx u 8 T,..-C\ns feo.ta.£ U/S w;lJ G'wded. BrotJ(j-.

-1 -
 . _,\

-2-
 Urological presentation
and investigation
.
, •
-
'
-·; ;

Done by : Bayan Al-Khd

5th year medical student , . - · .,..
- -v. '

\
.
..,
.

Urological presentation
**Patients with urological problems may
complain of many symptoms

**You should identify each symptom and make

analysis to have an idea about the cause of these
symptoms

1
•

-3-
 • Pain
o 1- pain:
dull pain in the loin area·
less dramatic in onset than uretric colic
not radiating to the external genetalia
mainly caused by stones
(infection ,inflammation ,obstruction )

2- uretric colic
intermittent , dramatic onset, no·relieving position
so severe: not relieved until the patient takes
narcotic

• Associated with nausea, vomiting and

· sweating
• Caused bv stones:
if in upper ureter radiates to groin
if in lower ureter radiates to scrotum and
external meatus and (to labia in females)

• if stone is close to VUJ the patient will have

irritation, frequency, and urgency
• 3- bladder pain: supra-pubic pain
• 4- prostatic pain: in the perineum/and or rectal
pam

-4-
 • 4- acute scrotum

sudden onset
of scrotal pain
is testicular
torsion until
proven
otherwise

Testicular Epididymo-
torsion orchitis
.w

'i·
J nset Sudden Gradual

CommonAge around 15 ys Elderly

l rine analysis -ve +ve

1 ss symptoms Vomiting Fever

( ihange in pain Relived No change

' elevation
( p:-emastric Absent Preserved
r flex

-5-
 Dysuria
(burning sensation) during micturition
Mainly due to initation of the urethra or
urinaJy bladder

Causes:
MC is infection or inflammation of the
bladder
Also could be psychogenic or due to reduced
VB compliance j

Hematuria:
May be microscopic (e.g. .renal or urinary tract disease)
macroscopic (e.g. hemorrhagic cystitis/bladder CA)
May be painful (e.g. calculi) or painless (e.g. malignancy).

RelaJionshiq between hematuria and voiding:

early hematuria: urethral
mid stream hematuria (total): urinary bladder and above
tennioal hematuria: prostate or bladder neck

color. bright red (recent) or dark (old)

causes of hematuria:
infecJious (UTI). stones, tumors (painless hematuria).
renal diseases (e.g. burger's glomerulonephritis},
bleeding disorders. vasculiJis

-6-
 Urinary incontinence:
Types of incontinence:
1- urge incontinence: results due to
involuntary rise in intravesical pressure
secondary to bladder contraction that
overcomes outlet resistance

causes:
loss of cortical inhibition( elderly,
parkinson's, MS)
local cause of detrusor
instability/overactivity (UTI, stones,
tumors, foreign bodies)

_?! •
.\ •
2-Stress incontinence
Leak of urine due to increase in intra-abdominal pressure
• at risk: elderly female, multiple pregnancies (weak pelvic floor), male
postTURP

• 3- overflow incontinence
• leak of urine a.fter prolonged obstruction and failure of the bladder to
empty
• MC associated with BPH and detrusor hypo-tonicity-secondary to
autonomic neuropathy (DM)

• 4- total (true/continual) incontinence

no control over the act of voiding
e.g. -injury to the external sphincter
-ectopic ureter opening distal to external sphincter
-congenital (e.g patent urachus, epispadius, ectopia vesicae)

-7-
 Enuusis
Involuntary wetting in children (espcx:ially nocturnal
bed-wetting)
Good cortical control of urination (inlubition) is achieved
at 2.5 years
2 types of enuresis
-primary. child was never able to attain control
-secoodary. child experienced control. then lost
(6 mon at least)

Polyurea
Normal urine output= 1.8 Uday
Polyure.a is tk.foted as an increase in total
volume ofurine >3 Uday
Caused by: DM(Izyperglycemi.a), diabetes
insipidus, chronic rCUll failure,
hypocalawniJJ, drugs (diuretics), psychogenic
polydipsia

Frequency
Normally people void at rate of4-8 times per day
Frequency is defined as an incresed rate of
miclwition without an increase ln the total volume
ofurine voided
Caused by: infections, metabolic disease,
psyclaogenic (anxiety)

-8-
 Urine retention:

Chronic:
Acute: •sua II)' usually paiD less
pablflllwithout 11idl renal
reual Impairment
lmpaJnnent

• auses:
• eebanical: BPH, prostate CA, prostitis
• eurological
• sychogenic

(}
i A'fP=' • Poor urinary stream
0
• Tested by uro-flowmeter in (ml/soc) normally >= 15 mllsoc
• 1be patient must have voided at least 200 ml during test

• Hesitancy:
• Difficulty to initiate urination
• (usu due to BOO e.g BPH)

• Dribbling:
• usu due to obstruction

-9-
Urgency

the feeling ofa sudden and immediate desire to void due

to irriUJLion ofthe urinary bladder or the urethra;
neurogenic bladder, pelvic organ prolapse
(overactive detrusor or abn. StretcJJ receptors in
bladder)

Nocturea
Defined as an increased number ofmicturition at
night (being awaked at night to void)
Caused by: -same causes as polyurea
-edematous state
-irritation : by infection, inflammation, or tumors

Oligurea
Defined by reuction in urine output to < 400
mllday
Extreme oligurea= Anurea= uriDe output <50
mVday
Causes : obsrruction,arterialorvenous
occlusion, acute renal failure

Pneumaturea
defined as passage of air bubbles with urine
Caused by internal fistula (e.g. vesico-colic fistula from
chrons or diverticular disease)

Cloudy urin.e
Caused by: infection (pyurea) and proticnurea(frothy)

-1 0-
·Laboratory investigation
• Blood
• CBC,KFT,

• Creatinine is better reflects kidney function than BUN

• Urine routine and microscopy (R&M)

• Routine: sugar protein, specific gravity, color, pH
• A.Ucal.ine mine indicates either infections or drugs
• Gluco:rurett occurs serum glucose>180 mg/dl

Microscopy: WBC (NL < per 3 HPF)

RBC (NL <2 per HPF)
• Epithelia cells, casts, bacteria

• Urine culture and sensitivity (Cd:S)

• -Culture: +ve if> 100,000/ ml in a clean sample or one
bacterial cell on microscope during R&M
• -sensitivity of the organism to various drugs

• Methods of sampling:
• -suprapubic (any single growth is significant)
• -midstream
• Catheter sampling

-11-
 • specific antigen (PSA)
• of high PSA.: infoctions, malignancy, BPH, trauma., pros2te
manipulation(PR.fulye' s)
• Causes oflow PSA.: prostatectomy, drugs (e.g. finasteride)

Normal values:
:1\ge: 60...69 yrs: NL free <0.9
PSA <= 4.5 nglml
NL total <4
Age: 50-59 yrs: Age: 40-49 yrs:
PSA<=3.5 PSA<=2.5
nglml nglml

• PSA velocity (i.e. rate of increase over time .. Must read at least 3
values in order to calculate)
• Normally= 0.04 ng/mJ/yr
If<= 0.2 ng/ml/yr probably
BPH
If>= 0.75 ng/ml/yr probably
prostate CA

• PSA fraction (ratio of free-to-total senun PSA)

• If ratio is <25-50% probably prostate CA

• PSA density (ratio of serum PSA to prostate volume)

• If>=O.l& nglmllcm• highly suggestive of malignancy
• PSA balflife (NL 2-3 days)
• If persist fur 3 weeks post prostatectomy... malignancy??
• Note.: 11ormal PSA anti nomud biopsy do not rule out prostate CA

10

-12-
lfJ Imaging studies
I 'N ••
......
K1J/! film (lddney-""''"-bladdul
• Look for aboonnal areas (e.g. radi<H>paque shadow, Psoas shadow,
bony metastasis

• Intravenous urogram (JV[J)/avp)

• Show intc:mal urinary tract as well as renal vasculature
• Must ask about radio contrast allergy and do a baseline KFT in
order- to avoid allergic reactions and death (occur 1 in 30,000 to
40,000)
• Must ask about Hx of pregnancy
• In case of anaphylactic rxn: ttt with adrenaline, antihistamioe, and
hydrocortisone (all IV)

,,
-13-
 • Procedwe i(WU
• Insert a large iv camrula
• First minute: nephrogram (shows kidney vasculature} then take
secj.al ncpbrogram
• Then take a full bladdr x-ray
• Finally take a post-void x-ray

• Signs o(tU:ute obstryction

• Dense cortex on ncphrogJaiD
• Hydronephrosis above the level of obstruction graded:

Minor : only dilation

Moderate: cupping of small calyces
Scveze: loss ofnonnal configuratio.n

• Filling defect DDX:

• Tumor,radioleucent stone, thrombus

• MictJnition cysto--urdhro-gram (MCUG)

• Contrast is injected into 'the bladder using a catheter and the patient
is asked ta void the contrast under flucoscopic vision
• Used to diagnose vesico-ureteric reflux (VUR)

• Ultrasound {US}
• Used to distinguish between cystic and solid masses
• For diagnosis of hydronephrosis
• Used to see post-void urine volume as well as to see the
VUJ,prostato size
• Stones only seen if>5 mm in size (esp renal stones)

12

-14-
• CT scan -+{ conJrast
• Usually we do aCT without contrast (esp ifcontrast allergy) yet a
contrast study is mandatory if there is a mass
• With CT: can see both radio-q>aque and ratio-lucent stones

• MRI
• Good Ia see soft tissue

• Retrograde ureterogrlllJhy
• Undec cystoscopic guidance, locate the ureteral orifices and inject
contrast into them
• Used to see dilated or obstructed ureters,strictures or injuries

13

-15-
 (J
1 Anterograde urethrograohy

N
'\:
0
Used to evaluate urologic strictures: size, length, and number of
strictmes

• Angiography
• To evaluate renal masses
• see a filling defects if the mass was cystic
• see abnonnal vessels if the mass was malignant
• To evaluate renal artery stenosis
• To evaluate vascular injuries to the kidney
• Lymplumgiography
• Less popular.. Replaced by CT-scan

• Scrotal U,IS -+1-

• Mandatory for scrotal pain and swelling to rule out torsion

14

-16-
 Radio nuclear studies
• 0
- • Types of radio nuclear scans:
• DMSA scan: Di-mercapto Succinic Acid
• DTPA scan (before renal transplantation)
• Hippurao scan: linked to iodioe-131 hippuran
• Perfusioo Radio-isotope scan
• Booe scan to evaluate for bony metastasis

• In DMSA & DTPA scans a radio-active substance is given IV and

the cortex is assessed for cortical functioning (used to see if the
cortex is scarred secondary to VUR)

15

-17-
 • Hippuran scan is used to asses obstruction in the setting of
significant renal failure. Here a graph showing flow and excretion
phases is produced:
• a-shows a normal vascular phase
• b-shows normal drainage phase
• c-shows slow flow: indicating renal artery stenosis
• D-shows slow drainage: indicating PUJ obstrucion

• Other diagnostic methods

• -cystoscopy: diagnostic and therapeutic

• -flowine1ry: shows rate of flow of urine
(urodynamic study)

16

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 17

-19-
-20-
 I )'.:r-)' r.
Sub-Surgery. Urology
1: Lecture topic: Urinary TB
• Date : 2009/20 10
Written by : Salwa AL-Bustanji

Urinary Tube.rculosis
'l./l.tfc.orLu.ctlon:
Q TB of the gerlitourinary tract is used by i\llycobacterium
Tubercuh)sis.

Was seen in but it is now increasing in

incidence in other ethnic groups.

Q ; ... ;ales>Females.

Clinicai symptoms usually develop 10-15 years aftei the

primary infection. Only about a quarter of patients with GUTS
have a known history of TB.

cJ'atltole.n.eJB:
:i.} Primary TB:

- Tile prim:::iry granulomatous iesi-:m forms in the rnid or upper

zone of the lung.

- ;..ccompanied by caseous lesions in the regional lymph nodes.

- Eventually, the thoracic duct may deliver mycobacteria to the

venous biood; this may rest.:lt in seeding of different organs,
including the kidneys.

- fo.riJ of TH bacilli through the blood stream to the

Bettitou,-inary tract.

P36

60

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- Immunity rapidly develops and the infection remains quiescent.

- Post Primary TB:

-Reactivation of infection triggered by immune compromise.

-At this point the patient deveiops clinical manifestations.

Jlfodj f)n. cflte #fli Omct:

• Kidney:

-The most commor. site of extrapulmonaryTB.

-Hematogenous spread causes granuioma formatio1=1 in the
renal cortex.
- In the kidneys, granulomas &re typically bilateral, cortical, and
adjacent to the glomeruli and may remain inactive for decades.

- Growing granuloma may erode into the calyceal system,

spreading the bacilli to the renal pelvis, ureters, bladder, and
other genitourinary organs.

- caseous necrosis of the renal papillae and deformity of the

calyces.

- -passage of bacilli in the urin2.

- -Healing by fibrosis and calcification

- -Destruc.tion of the renal architecture and autonephrectomy.

- -Although both kidneys are seeded, clinically significant disease

usually develops in only one kidney.

• Ureters:

-Direct spread from the kidney.

61

-22-
 -genera II'/ to the ureterovesical junction. It only rarely affects
the middle third of the ureter. ·
-Stricture formation:vesicoureteric junction, pelviureteric
junction, and midureteric.
-ureteritis cystica.

• Bladder:·

-usually secondary to renal infection.

-Can be iatrogenic due to intravesical BCG treatment for
bladder CA.
-usually starts at the ureteral ocifi.ce.
- The bladder wall becomes red, edematous, and inflamed with
ulcerations and tubercles;yellow lesions with a red hallow.

- Disease progression causes tbrosis and contraction,

obstruction, calcification, and fistula formation.

P( ...:.si:ate and Seminal vesicles:

-Haematogenous spread causes cavitation and calcification,

\'lith palpable, hard-feeling structures.
-Fistulae may form to the rectum or perineum.
- Decreased semen volume may indicate extensive prostatic
disease 01 ejaculatory duct obstruction.

• Epididymis:

-Descending renal infection or hematogenous spread (more in

children )
-3eaded cord, which m.ay be tender or asymptomatic, and is
usually unilateral.
Abcess, spread of infection to the testis, or
infertility.

• Tescis:

62

-23-
 -Infertility may result from bilateral vasal obstruction.
-Orchitis and the resulting testicular swelling can be difficult to
. of the testes.
differentiate from other. mass lesions

o Symptoms are generally chronic, intermittent, and nonspecific.

• The most common age at presentation is 30-45 years.

o Early symptoms: fever, lethargy, weight loss, night sweats, and

UTI not responding to ..

o later mailifestations: LUTS, haematuria, and flank pain.

a Hematuria :gross, painless in 10% of cases. Microscopic

hematuria is present in 50% of cases.

• Physical examination: Tende-r testicular or epididymal swelling,

beading of the spermatic sinus
formations may develop.

Cln.Vtdt.atlom:
o Urine:-

.-at least 3 early morning urine samples are required, but often
many more E;v1U spe.:imens -_·iii! be needed before a positive
culturE:: for TB is obtained.
- A typical ftnding is sterile pyuria (leucocytes, but no growth).
- Ziehl -Neelsen staining wiil identify these acid- and alcohol-
fast bacilii (cultured on Lowenstein-Jensen medium).
• CXR and sputum.

• Tuberculin skin test.

P39

63

-24-
 o IVU: findings include renal calcification, irregular calyces,
infundibular stenosis, cavitation, pelviureteric and
vesicoureteric obstruction, and a contracted, calcified bladder.

o Cystoscopy and biopsy •

.0 'Ce.a:tmen.t:
o An initial phase of 2 months of isoniazid, rifampicin,
and ethambutol followed by a continuation
phase months of isoniazid and rifampicin.

• Longer treatments or modification ot medications is needed for

compllcations resistant organisms.

o Non-functioning, calcified kidney may need nephrectomy.

• Regular follow-UfJ imaging with IVU is recommended to

monitor for ureteric strictures, which may need stenting,
nephrustomies, or ureteric reimplantation.

o Severe bl3dder disease may require surgical augmentation,

reconstruction, or urit.ary Jiversion or cystectomy and
neobladder recunstruction.

Epididymectomy+\- orchidectomy is considered if

pharmacotherapy fails or extensive disease is present.

• Good:

o Early detection of disease

o Young age

o Sensitivity to first-line me::!ications

P40

64

- 25-
 Absence uf comorbid conditions

o Compliance with medications and follow-up care

• Poor:

o late detection with complications

o low socioeconomic group

o Old age

o Other imrnunocorr.promising conditions

GOOD lUCK ....

--

.....

65

-26-
 UrinaryTB
(ADDITIONS)

+ Renal1B: (hematogenous spread/ also it is the most common extra

pulmonary TB/ slow progressive Ds).

+ Active renal+ pulmonary 1B together in 4- 8 %only.

+ Ifpatient with ureteral TB, the kidney i.s always involved.
+ Usually starts to be symptomatic when it causes (tuberculosis cystitis}.
+ common question -7 prostate and seminal TB (Hematogenous OR
descending rout).

+ More common in males

**Think in urinary TB:

1. HxofTB.

2. Failure to response.
3. Sterile pyuria.

4. Micro hematuria with no cause.

5. Multi- indurations.

6. Draining Sinus (pathomnemonicto Kidney)

... 66
...............................................................
-27-
-28-
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85

-29-
86
-30-
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P57

87

-31-
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88

-32-
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89

-33-
 Pediatric Urology
1. Testicular

• In the 7th month of gestation, the testicles normally descend into

the scrotum. Continued descent of the testis may progress after
birth, but descent comes to a halt before 2 years of age: .
• In up to 4% of normal full-term newborn males, one or both testes
have failed to reach the scrotum, and this percentage increases with
prematurity (30%).
• By the age of one year, full descent will occur in most boys,
leaving about 0.3% with testes. (A !_esticle is
considered truly undescended at the age of OJie year.)
a The cause of most cases of cryptorchidism is unknown, but a
deficiency of androgen production by the fetal testes is an
important factor.
II The maldescended testes may be arrested at any point on its path of
descent from the posterior abdominal wall to the scrotum.
Q Abdominal.
Inguinal canal.
Q At the external ring (the most common).
9 Perineal.
• Superficial inguinal pouch.
• High retractile..
8 The right testis is affected in 45% of cases, the left.in 30%, and
both testis in 25%.

• Complications
• Testicular malignancy (especially seminoma).
• There is a 30 times increased risk.
• Surgical correction doesn't reduce this risk; however, a
testicular tumor is more likely to be discovered early ifthe
testis is in the scrotum.
• Subfertility:
• Nonnal spermatogenesis requires the cooler temperature
of the scrotum. Unless the disorder is corrected, all
bilaterally cryptorchid adult males become sterile.
• Traumatic injury.
• Torsion. 5:

P60

90

-34-
 8 Patent processus vaginalis is present in 95% of patients with
cryptorchidism, and approximately 25% develop a clinical hernia.
D Anomalies associated with cryptorchidism occur in about 15% of
cases and include a wide variety of syndromes as: Klinefelter
syndrome, hypogonadotz:opic hypogonadism, renal agenesis, horse
-shoe kidneys, extrophy of the bladder, ureteral reflux and others.
• Physical examination demonstrates an empty hemiscrotum with
absent rugae.

• Treatment
• Surgical correction (orchidopexy):
• This is best performed before the age of2 years.
• The usual technique involves
o Mobilizing the spermatic cord.
o Placing the testes in a subcutaneous serotal
pouch outside the dartos muscle. ·

Retractile testes
II Here, the testes don't appear to be fully descended, and can be
palpated-in the scrotal neck and gently manipulated into its correct
position.
M It is due to the very active cremaster muscle in children under 3
years of age and the small testis. It is a variant of normal.
I! This requires no treatment provided the testes become Jess
retractile as the boy grows.

·.

Pol

91
I .

-35-
 2. Ve§icoureteric Reflux
Normal physiology
• The main function ofthe.ureterovesicaljunction is to permit free
drainage of the ureter and simultaneously prevent urine from refluxing
back from the bladder.

• The ureteral musculature continues uninterrupted into the base of the

bladder to form the superficial trigone, and this direct continuity offers
an efficient, muscularly active valvular function. Thus, any stretch of the
trigone (with bladder fllling). or any trigonal contraction (with voiding)
leads to firm occlu5ion of the intravesical ureter, and prevent retrograde
flow.

Etiology
• Primary VUR
e Developmental ureterotrigonal weakness.
• Ureteral anomalies
• Ectopic ureter.
e Duplex ureter.
e Congenital megaureter.
• Ureterocele.

• Secondary VUR
• Bladder outlet or urethral obstruction.
o Neuropathic dysfW\ction.
o Iatrogenic causes.
• Infection, e.g., TB.
0 Stones and foreign body.

Complication
• Pyelonephritis.
• UTI.
• End stage renal

P62 t

92

-36-
Clinical findine:s
e Infants and young children
• Non specific symptoms (due to UTI)
./ Vomiting.
../ Fever.
./ Failure to thrive.
Older children
• Incintinence.
• Frequecny.
• Dysuria.
• AOdominal pain.
e With acute pyelonephritis
• Fever and chills.
• Costovertebral angle tenderness.

Diagnosis
• Urinalysis and urine cultures
• Evidence of infection; pyuria and bacteriuria.

o Abnormal renal function tests.

,_ Radionuclide voiding studies.

a Voiding cystourethrogram

• This is the standard investigation; it demonstrates the grade

of the reflux and the urethral anatomy.
• This involves injecting CQJttrast medium into the bladder via
a urinary catheter, the catheter is then removed and :x. - rays
are taken while the child is voiding;
./ Grade I -reflux into a nond.ilated distal ureter.

./ Grade II- reflux into the upper collecting system without

dilation .
./ Grade III- reflux into a dilated collecting system without
blunting of calyces .
./ Grade IV- reflux into a dilated system with blunting of
calyces.
./ Grade V- massive reflux with gross dilation and distortion
. of the ureter and collecting system.
(Pedialrics recall page 299)

-
Po3

93

-37-
 Management
G When there is no ureteral dilation, there is an 85% chanee of
spontaneous resolution as the child grows. In the meantime, the urinary
tract must be kept free of infection, and this is done by:
• Regular voiding. ·
• High fluid intake.
• Avoiding constipation.
• Maintaining perineal hygiene.
• Anti -bacterial chemotherapy.
• Regular follow up, with charting of growth and development.

• In obstructive secondary reflux (e.g.• posterior urethral valves), release

of obstruction may cure reflux.

o In neuropathic reflux, intermittent catheterization fir control of infection

may allow return of valvular competence.

• Surgical correction and this is done by reimplanting the ureter in the

bladder wall so that a length of it lies deep to the bladder mucosa. This
is indicated for:
• .severe reflux with dilated ureters.
• For other anatomical abnormalities.
• For children who fail to progress on consrevative management.

3. Ureteral anomalies

• Congenital obstruction of the ureter.

• Duplication of ureters.

• Ectopic ureteral orifice.

• Ureterocele.

-
P64

94

-38-
4. Bladder. anomalies
0 Bladder agenesis.

Q Bladder·duplication.
m Complete; with sepirrate urethral openings drained by duplicated
urethras.
!!I Incomplete; with a septum defonnity.

0 Urachal anomalies
8 Urachal diverticulum.
II Urachal cyst.

e Extrophy_of the bladder

• It results from a complete ventral defect of the urogenital-5inus and

the overlying inferior abdominal wall musculature.

• Presentation:
-/ The lower central portion is devoid of skin and muscles.
-/ The anterior bladder wall is absent, and the posterior wall
is contiguous with the surrounding skin.
../ The rami ofthe pubic bone are widely separated, and the
open pelvic ring may affect gail
../ Urine drains onto the abdominal wall.
-/ In males, the penis is shortened, and the urethra is
epispadiac.
-/ The exposed bladder mucosa tends to be chronically
inflamed.

• Treatment: .
-/ Closure of the bladder in the newborn period.
-/ Urethral closure and penile reconstruction.
-/ Ureteral reimplantation.

P65'

95

-39-
 5. Penile and urethral anomalies
A. Hypospadias.
• It results from failure of fusion ofthe urethral folds on the undersurface
of the genital
• Incidence: 1 in 400 male bi.rths.
• The urethral meatus is ventrally displaced on
• The glans.
• The sbaft of the penis.
• The level of the scrotum.
• The perineum.
• The remnant of urethral tissue distal to the meatus is fibrotic, causing
the penis to bend downwards or (chordee). The plQ.re proximal
the urethral meatus, the worse is the chordee.
• The ventral part of the foreskin is absent giving rise to a hooded
appearance.
• In Hypospadias with the meatus positioned proximal to the
circumcision shouldn't be done; as the prepuce can be used later in
surgical repair.
• Management
• If the opening is glandular or coronal (85%), the penis jg usually
functional, and repair is done pri..marJy for cosmetic reasons.
• More proximal openings require correction (surgical plastic
repair).
• Compicatios of surgery
• Meatal stenosis.
• Fistula formation.

B. Epispadius.
• Here, the urethra opens on the dorsum of the penis, with deficient corpus
and loosely attached corpora cavemosa.
• If the defect is extensive, it may extend to the bladder neck causing
incontinence.
• The pubic bones are separated, as in extrophy.
• Marked dorsiflexion of the penis is usually present.
• It is commonly associated with bladder extrophy, and if present alone is
considered as a mild degree of the extrophy complex.
• Treatment:
• Correction of penile curvature.
• Reconstruction of the urethra and bladder neck.

P.GA

96

-40-
 C. tJrethral strictures.
• Most common in the fossa navicularis Gust proximal to the
meatus), and in the bulbomembranaous urethra.

• They are thin diaphtagms that respond to simple dilation or direct

visiop internal urethrotomy, and rarely open surgery is required

D.Posterior urethral valves.

• The most common obstructive urethral lesions in newborn and infant
males, and the most common cause of end- stage renal disease in boys.
• They are obstructive mucosal folds, seen only in which originate
at the veru montanum at the prostatic urethra. ·

• Clinical manifestations:
•!• Difficult voiding.
•:• Week stream.
•!• A lower abdominal mass that represents a distended
bladder.
•!• Palpable kidneys with signs of acidosis and uremia
•:• Urinary incontinence and UTI.
·!• Up to 70% have VUR

• Laboratory fmdiogs:
•:• Elevated BUN and creatinine.
•:. Evidence of UTI.
•:• U/S shows evidence of bladder thickening and
trabeculation, hydroureter and hydronephrosis.
•:• Voiding cystourethrogram demonstrating the urethral
valves eotabUshes the diagnosis.

• Treatment:
•:• Endoscopic destruction of the valves as soon as possible.

--- ---

v- If: -;:v.

Essential surgery, jnl chapter 45•

,,.. . .
,,

97

-4 1-
-42-
 i. Pretesticular causes
IB Hypothalamic disease
I. K.allmann syndromes
a Isolated gonadotropin deficiency ''absent GnRH"
11 Associated with anosmia.
4- Isolated LH deficiency.
3. Isolated FSH deficiency.
4. Prader- willi syndrome
• Excessive eating and obesity.
• Sexual infantilism.
• Mental retardation.
• Short stature
00 Pituitary disease
1. Pituitary tumors.
../ Pituitary adenoma
• Hyperprolactenemia.
• Loss oflibido and impotence.
o Gynecomastia and galactorrhea.
• Visual field defects and headaches.
2. Infection.
3. ·Iatrogenic; surgery, radiation.
4..Hemochromatosis
-/ Testicular dysfunction.is found in 80% of patients due
to iron deposits in the liver, testis, or the pituitary.
1&1 Exogenous or endogenous hormones (bysuppnnincpiluiwnonado!roriru)
1. Estrogen or androgen excess
• Adrenocortical tumors.
• Sertoli cell tumors.
• Hepatic cirrhosis.
• Exogenous androgens "anabolic steroids..
• Congenital adrenal hyperplasia
• Defective 21 - hydroxy lase enzyme --- defective
cortisol synthesis --- increased production of
androgenic steroids.
• Premature development of secondary sexual
characteristics.
• Abnonnal phallic enlargement.
2. Glucocorticoid excess.
• Exogenous; treatment of asthma, UC and RA ...
· • Endogenous; cushing syndrome
3. Hyper- and hypothyroidism

P109

191

-43-
 .ti. Testicular causes

1. Chromosomal abnormalities
A. Klinfelter syndrome.
../ An extra x chromosome in a male (47 XXY) .
../ Incidence 1:500 males.
v' Small and firm testis•
../ Delayed sexual maturation.
.,/ AzoospertJlia.
../ Gynecomastia.
B. Noonan JYildrome (male turner syndrome)
../ Short stature•
../ Webbed neck.
Low- set ears.
Cardiovascular abnorMalities.
2. Bilateral anorchia (vanishing testis syndrome)
Non- palpable testis.
Sexual imhlaturity._
-1' Low testosterone levels.
-1' Elevated FSH and LH levels.
3. Gonadotoxins
0 Drug5
• Chemotherapy.
• Ketoconazole
• Spironolactone.
• Cimitidene.
• Alcohol, heroin, methadone and marijuana.

0 Radiation
> Germ cells are particularly sensitive to radiation, while Jeydig
cells are relatively resistant.
4. Orchitis
• 15 - 25 % of adult men who contract mumps (parotitis) develop
orchitits which is commonly unilateral
• Testicular atrophy can within months or may take longer
years.
5. Trauma
• Iatrogenic injury during inguin8l or scrotal surgery.

6. Cryptorchidism
• 0.8% of adult males.
• Most men with unilateral undescended testis are fertile.

P1 "1"0'

192

-44-
 7. Systemic disease
A. Renal failure.
IJ Uremia is associated with decreased libido, impotence, altered
spermatogenesis aod gynecomastia.
• This is due to
!I Increa.Sed prolactin and estrogen levels.
11 Medications.
r! Uremic neurop.athy.

B. Liver cirrhosis.
1!!1 Testicular atrorby, impotence and gynecomastia.
• Decreased hepatic extraction of androgens - increased
conversion to estrogen..

C. Sickle cell disease.

8. Varicocele
o Abnormal dilation of the veins of the pampiniform plexus in the
spermatic cords. It is described as a bag of worms.
o It results from backflow of blood secondazy to incompetent or absent
valves in the spermatic veins.
o 90 o/o of varicoceles are on the left side, and this id because
• The long vertical course of the left internal spermatic vein,
where this vein runs obliquely on the right side.
• The left testicular vein drains into the high pressure renal vein,
while the right one into the IVC.
o A unilateral right sided varicocele suggests venous thrombosis (e.g.
tumor) or situs inversus.
o 40 % of varicoceles are bilateral.
o Incidence:
• 10- 15% in adult males.
• 20-40% in individuals evaluated for infertility.
o 50 % of men with varicoceles will have impaired semen quality, but
many men are fertile.
o Varicoceles icrease scrotal temperature which may inhibit normal
sperm function end eventually cause testicular atrophy.

-
P111

193
.. .... .:...

-45-
 ill. Post testicular causes

1. Disorders of transport
A. Congenital disorders.
Iii Absent vas deferens, ampulla or seminal vesicles.
B. obstruction. .
m Pelvic surgery- nerve injury and a peristaltic vas
def. .
Diabetic males with autonomic neuropathy.
& Spinal cord lesions.

2. Disorders of sperm motility or function

A. Kartagner syndrome. . _
Chronic sinusitis and bronciactasi.s.
£ii Situs inversus.
g Immotile sperm.

B. Sexual dysfunctjon.
a Decreaied sexual.desire.
6 Impotence.
g Premature ejaculation.
C. Infectios, e.g., STDs.

P112

194

-46-
 Workup

B Semen analysis
I! At least 3 samples should be taken.over a 2- month period.
B Semen should be collected by masturbation, after 48 - 72 hours of
abstinence, and analyzed within an hoUr' of collection with being kept
at body temperature.
II Normal values are:

Volume 2.5 to 6 m.l

More than 20 million per cc.

!motility iMore than 50 % with forward progression

- -
WBCs IFewer than I million/cc
morpblogy More than 50 % normal

Other criteria in the semen

•:• Fructose.
• It is produced in the seminal vesicles and thus reflects
its function.

•:• Coagulation
o Normally, the semen coagulates and then over the next 5 to 20
minutes liquefies.
o Delayed liquefaction (more than 60 min.) reflects accessory
_glands dysfunction.

• Post coital test

• The mucus is examined 2 to 12 hours after coitus for total number of
spenn seen per high power field and percentagC\ "-..d quality of motility.
• A satisfactory test is one in which more than 10 motile spermatozoa
are seen per HPF.
• Non motile spermatozoa may be the result of:
• Azoospermia.
• Inherent poor spematozoal motility.
• Hostile cevical mucus.
• Poor coital teqnique.
• Small ejaculate yolume.

P113

195

-47-
 a Sperm antibodies (in the man or woman)
o These have been reported in 3 -7% of infertile men.
o Possible etiologic causes:
o Previous inflanlniation to the GU tract.
• Testicular injury or torsion.
• Previous vasectomy.

a Hormonal evaluation.
o LH, FSH, and testosterone.
o ACTH, TSH. and GH.
0 Prolactin.
• Testicular biopsy.
D Chromosomal studies.
II Sperm function tests
o Sperm - cervical mucus interaction.
o Sperm penetration assay.

Treatment
• Medical therapy.
ii Endocrine therapy .
Ill Immunologic infertility: steroids.
• Retrograde ejaculation
o Here, the bladder neck fails to close during ejacuiation.
o Alpha- stimulation with sympathomimetics.
o Alkalization of the bladder urine witi oral NaHC03 and retrieval
of sperm from the bladder after ejaculation has been successfully
used for artificial insemination.
• Treatment of infection.
• Correction of coital factor
o Psycotherapy.
o SexUal therapy.

• Surgical therapy.
o Reversal of sterilization.
o Varicocele surgery.
• Assisted reproductive technology.
·o IVF.
o Int.aruterine insemination (IUI) of washed spermatozoa.
o Gamete intnUallopian trans(er (GIFT).
o Intracytoplasmic s,erm. injection

P114

196

-48-
 Pediatric urology/ OSCE notes
Dr. Saddam Dmour

OSCE station

You are the pediatric resident in the ER, there is a child presented with fever.

What is your differential diagnosis ?

There are many causes of fever in children like gastroenteritis, URTI, pneumonia and UTI
(long list; you can mention many others)

What are the urology-related causes in this age ?

There are three and you have to mention all of them :
Vesicouretral reflux.
Posterior urethral valve.
PUJ obstruction.

What is your management plan for this patient ?

History, physical exam and investigations.
You start with basic and simple lab tests like CBC, blood culture, urine analysis and urine
culture and then, according to the history, PE and the lab results you may need further
investigations, for example if you suspect vesicouretral reflux (Hx of recurrent UTI and
positive urine culture) you should do voiding cystourethrogram (VCUG).

Vesicourethral reflux (VUR) is also an important topic in pediatric urology for OSCE exam
Common questions :
What are the classification of VUR ?
Primary VUR.
Secondary VUR.

What is the most common cause of secondary VUR ?

Neurogenic bladder.

What is the management ?

Primary VUR is surgically corrected.
Secondary VUR you should treat the cause.

You should know the grading ofVUR and when surgery is necessary.

Good luck©
Done by Hiba Smadi

- 49-
-50-
 URINARY
INCONTINENCE

lnl1b1ed
!causes
conhdi:xl)
5linUD!d
f';alses

So.Cnm Wiled

contactllnl

FIGURE 16-11
Control a

201

-51-
 DEFINITION ·
*Involuntary loss of urine

*Failure to store urine during the filling

phase

*Urine loss ,urethral or extra-urethral

*major health issue that affects more than

million people worldwide

*Overall prevalence of female

*incontinence increasing with age from 20-30%

during young adult life to almost 50°/o in
the elderly

202

-52-
DETRUSOR OVERACTIVITY

203

-53-
 LOW BLADDER COMPLIANCE

Decreased volume to pressure relationship •

Causes: 1) Neurogenic (ms tone):
spinal cord injury,
radical hysterectomy
2) Increased collagen (elasticity): cystitis,
chronic indwelling catheter, prostatic
obstruction

URETHRAL HYPERMOBILITY
**Due to a weakness of pelvic
floor support

**Leads to a rotationat descent of

the bladder neck and proximal
urethra during increases in intra-
abdominal pressure

204

-54-
INTRINSIC SPHINCTER
DEFICIENCY

RISK FACTORS

205

-55-
 Type of htcoutiDe.Dc:e Deftnltioa Cause

Stress IDvoluatary loss of urlne Hyper mobWty of tb e

due to U.cnued latra- veslcourethral or
abdominal pnssure pelvic floor wealmess

Uqe IDvollmtary lou of urfae, Detrusor lnstabOlty or

lmmedlately pnuded by spblacter lnsUbOJty
•reeacy
<hluflow lllvoluntary loss of urlne Bladder outlet
with bladder O"VH obstnlctioa or laadeqvate
dlsteadon bladder
Mixed Stnu rda.ted uriaary
lacoutloence wtth
•J'Ieocy

Functional incontinence
seen in patients with normal voiding systems but who have
difficulty reaching the toilet because of physical or
psychological problems. Patients often present with
recent symptom onset and have a good prognosis for
cure if the cause is identified and treated

oTotal incontinence
Constant diurnal and nocturnal incontinence without normal
voiding.
Causes:
-fistula
-injury to external sphincter
-ectopic uretral opening
-epispedias
-radical prostatectomy

206

-56-
 Evaluation
History:
ask your pt about
- LUTS,
-triggers for incontinence,
-frequency and severity of symptoms
-establish risk factors.

Physical Examination
-speculum examination
-bimanual pelvic exam
-rectal exam
-Ask the patient to cough and inspect for vaginal wall
prolapse and urinary leakage
- Examine the abdomen for a palpable bladder
-Neurological exam:
Deep tendon reflexes
Anal sphincter
Pelvic floor contractions

..

207

• ·---· ·- - - • - ___. J. ' . .:-.· · ........ .

-57-
 INVESTIGATIONS
-Urine culture and analySis
-Standing stress test
-Pad tests
-Cotton swab test (Place a sterile swab
through the urethra into the bladder. Pull the swab
back until resistance is met, which indicates entry
into the urethra. At this point, ask the patient to strain
maximally.
A change o(angle greater than 30 degrees indicates
urethral hypermobilitv.)

Urodynamic studies •
-Cystometrogram
-Residual urine volwne
-Bladder capacity and sensation
-Involuntary dtruser contractions

. - :
if suspecting fistula (methylerie blue test or· •
cystourethroscopy )

208

-58-
Conservative :
Pelvic floor exercises
Life style moclification

Medication:- -
1) Anticbolinergics: inhibit bladder contractions and lnc.rea.c;e -
capacity
e.g. oxybutynin. tolterodine,
trosplum, proplver

2) Intravesical botulinum toxin A

3) Drugs for urethral incompetence

pseudoephedrine
phenylpropanolamine
Estrogen

4 ) drugs to treat overflow incontinence

prazosin ,terazosin
Dantrolene
Bethanecol

209

-59-
 Surgical:
1) Sphincteric incompetence
Intra -urethral and bladder neck injections
Retro-pubic suspension

Vaginal procedures

Artificial urinary sphincters

2) Diminshed bladder capacity

Augmentation cystoplasty
Urinary diversion

3) Intennittent" catheterization
4) Indwelling urethral catheter
5) Fistula repair

210

-60-
A B

211

-61-
 surgery ktbe treatment of choice for stress incontinence
.(risk of failure is 10-20%)

-medical treatment for urge incontinence is.successful in

50-80% (no role for surgery)

TH-ANk
yoVl
"

212

-62-
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 Urology
2014-2015

Those are some important notes you need to refer to them as they are not covered in the
dossier of our colleague Sarah Ghaith.

Renal trauma
Lecturer: Dr. Mujalli Muhilan

Kidney trauma

*Fascia of Gerota
-It's a strong layer of fascia surround the kidney.
-Because of the presence of this fascia, many of closed kidney injuries are treated
conservatively, so it's very important.
-It induces a tamponading effect during injuries which helps in reduction of bleeding.
-Spleen and liver don't have a fascia like this.

*Contents of the hilum (pedicle) of the kidney

-7 From posterior to anterior :
-Pelvicalyceal system and ureter.
-Renal artery
-Renal vein (the most anterior structure)

*Deceleration injuries
These injuries occur due to the difference in velocity between the body and the kidney at
the time of injury (during a car accident for example)
The difference in velocity will lead to shearing force which will induce a lot of damage in
the pedicle that attaches kidney to its blood supply, so deceleration injuries are very serious.

*Management
-Management of the majority of closed kidney injuries is conservative.

-Indications for surgery in closed kidney injuries :

1) Failure of conservative treatment as judge by the PULSE in spite of fluid management.
(note that pulse is the most important vital sign used here to judge on the failure of
conservative treatment)
2) Continuous blood loss (unstable).

-99-
3) Grade IV and V because the patient here is unstable from the beginning.
4) If there's tachycardia followed by

-All penetrating injuries need exploration, because that the degree of injury doesn't correlate
with the amount of the damage that has occured especially if we are talking about high
velocity injuries (gunshot injury for example).

-All open kidney injuries need exploration.

*Late complications of kidney injures (as mentioned by the Dr) :

1) Scarring of the kidney (this is irreversible)
2) Renal artery stenosis
3) Renal artery aneurysm
Regarding the complications in points 2 and 3 :
In both cases the patient presented with HTN
You should detect tliem because both are treatable.
4) Traumatic PUJ.
5) Urinoma (leakage of urine surrounded by a fibrous capsule).

Uretral trauma

-Ureter is found anterior to the bifurcation of common iliac artery which is an important
land mark for us.
-Uretral injuries are NOT rare.
-Nowadays, most common uretric injuries are due to uretric manipulations like DJ and
uretroscopy (mainly used in treatment of stone diseases).
-Uretral trauma are either simple or complex.

-Simple uretric trauma

Simple uretric trauma are classified into :
-7 Simple uretric trauma without distal obstruction
No treatment is needed here.
-7 Simple uretric trauma with distal obstruction
Either you remove the obstruction agent or bypass it.

-Management of complex uretric trauma :

End to end anastomosis should be done, if you can't do it you have to reimplant the ureter
any where you get access to the bladder (not necessarily at the vesicouretric junction).

-100-
Bladder trauma

-Bladder dome/apex is the only intrapertonial part of the bladder.

-Baldder injuries are either intrapertonial or extrapertonial.

* Intrapertonial bladder injuries management:

All of them need surgical intervention (lapartomy and clouser of the perforation)

* Extrapertonial bladder injuries

Those are less drastic than intapertonial injuries.
They are classified according to severity into mild, moderate and severe injuries.
Mild injuries
-Like in cases of tumors when you take a biopsy, if you go deep you may cause a mild
injury to the bladder (in this case you know that you perforate the bladder when you see
FAT; yellowish discoloration)
-Management of mild extrapertonial bladder injuries :
Catheterization

Moderate injuries
-Management of moderate extrapertonial bladder injuries :
Catheterization and supra-pubic drainage.

Severe injuries
-Management of severe extrapertonial bladder injuries:
Treat it as intrapertonial injuries.

Urethral trauma

-Female urethra is short (4 em) and well protected so urethral injuries are rare in females.

-Male urethral injuries are divided into :

1) Injuries of penile urethra
Important but less drastic
2) Injuries of prostatic urethra
Not significant
3) Injuries of membranous urethra (external sphincter injury)
The WORST urethral injury.

-101-
Endoscopically, the land mark of this injury is verumontanum (the opening of ejaculatory
duct)
If there's an injury to the external sphincter either by trauma or TURP the patient will be
totally incontinent.

Presentation of a patient with urethral injury

Small trauma
The patient presented with hematuria, don't touch him because his condition will become
worse and as a result the patient will become incontinent if you interfere.

Serious trauma
- Like in the case of transaction of urethra at the membranous part.
- C!P in this case :
1) Acute urinary retention (the patient will not be able to void at all)
2) Bleeding per urethra (NOT HEMATURIA)
3) Perineal brusing.

-Our priority here is to know if the two segments still in a straight line or not, How?
1) By doing PR, if you feel the prostate still in place then the two segments are still in line,
if not, then there's malalignment.
2) By doing ascending urethrography (aseptic urethral x-ray imaging)
Here you give a contrast through the urethra if it goes to the bladder (as shown by x-ray),
then the two segments are in line, if not, then there's malalignment.

Now, how to manage this patient?

If the two segments are in line you just have to do supra-pubic catheterization.
If there's malalignment, you have to put the two segments in one line by Railroding
technique.

Follow the patient up after urethral injuries for :

1) Urethral stricture
2) Incontinence

-102-
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-116-
 Testicular cancer
Lecturer: Dr. Adel AI-Rabadi

Testicular cancer is RARE and has a good prognosis if diagnosed early.

There are many factors that determine if testicular cancer will be diagnosed early or late; we
can divide them into two categories; patient factors and physician factors :
Patient factors:
1) Embracement
2) Cultural and sexual education of the patient; some patient may consider the enlargement
in testiclular size (which occurs in testicular cancer) as a part of normal sexual
development.
3) There's scrotal self exam (like that of the breast) but it's not well known in the society.
Physician factors:
1) The Dr didn't do full physical examination, remember this, abdominal examination is not
complete if you didn't examine the genitalia.
2) Wrong diagnosis; for example testicular hydrocele sometimes mask the pathology of
testicular cancer, some doctors simply diagnose it as hydrocele although it may be
secondary to testicular cancer. Also if this hydrocele is tense, it will impare proper
diagnosis so your PE should be followed by U/S.

Presentation of any scrotal pathology is either mass or pain or both of them.

Since testicular cancer can be presented with mass or pain or both of them you should keep
it in your differential diagnosis list whatever the scrotal complain is.
Testicular pain is either acute (severe) or chronic (dull aching).
Acute testicular pain results from either infarction or hemorrhage.

Gynecomastia occurs by the effect of complex hormonal interaction; not purely by

BHCG.

Testicular cancer can be presented with hyperthyroidism (TSH and hCG are similar
enough).

Ddx of testicular cancer differs according to patients' age and clinical presentation. So if a
25 year old patient presented to ER with acute severe scrotal pain, what is your ddx ?
In this case, your list should include : torsion, epididymitis and testicular cancer. varicocele
is not acceptable to be in your list here.
Another example, what's your ddx for testicular pain of2 months duration ?
Here, think of varicocele > hydrocele > testicular cancer.

- 117-
Testicular cancer and tumor markers:
really rare to see an isolated type of testicular cancer.
is a% of testicular cancer with normal levels of tumor markers.
level of tumor markers doesn't r/o testicular cancer but if there's an abnormal
this goes with our diagnosis of testicular cancer.
markers are not specific.
levels ofB-HCG are not found in teratoma.
LDH is very non-specific, it's mainly used to determine tumor burden (size). High tumor
burden usually associated with high level of LDH.

Lymphatic drainage of scrotum differs from that oftestes; lymphatic drainage of scrotum is
through inguinal lymph nodes while testicular lymphatic drainage is through para-aortic
lymph nodes.
So the regional lymph nodes that are involved in cases of testicular cancer are para-aortic
lymph nodes not inguinal (final exam question).
Except for choriocarcinoma (which is a very bad tumor, the only type that likes
hematogenous spread. Usually there is a small mass but with mets to liver and lungs so the
pt is unlucky here.) , testicular cancer has a stepwise lymphatic metastasis (no skipping) this
means that the first lymph node to be affected will be para-aortic, then from there it descend
to common iliac LNs and from there it descend to the lymph nodes around the internal and
external branches of common iliac artery. If mets occur in external branch and from there it
descend to femoral LNs it will end up in inguinal LNs. So that inguinal LNs involvement in
testicular cancer occurs late in the disease (advanced stage).

If a pt with testicular cancer presented with inguinal LNs enlargement you can think
of:
stage of testicular cancer.
may be unrelated to the cancer; infection for example.
cancer with scrotal involvement
patient has a previous scrotal surgery which cause disruption of lymphatics.

General notes regarding testicular cancer :

step in management of any type is radical inguinal orchitomy, then you send it for
histopathology and do staging.
of testicular cancer depends on the type and the stage of the tumor.
types of biopsy are contraindicated in the diagnosis of testicular cancer.
solid testicular mass should be managed as malignancy until proven otherwise and
histopathology should always be done.

-1 18-
 patients with single testes, if you suspect cancer you can use frozen section approach
and do partial orchitomy if possible.
packing should be done before orchitomy for patients with single testes and also
for those with bilateral testes because you will give RTX and CTX after surgery.
cancer in general has an excellent response to CTX even ifthere's metastasis.

Seminoma:
a histopathological diagnosis.
25-35.
bilateral.
in a very nice way to RTX.
surgery, the 2"d line in managment is RTX and the 3rd line is CTX.

RPLND:
a major surgery that involves removal of LNs from level of renal artery then from
level of ureters and then at bifurcation of iliac vessels.
has a lot of complications with high morbidity.
Reterograde ejaculation is one of the complication, because of damage of sympathetic
innervation during surgery. In order to avoid this we do what's known as modified RPLND
in which we spare one side of sympathetic innervation and this will preserve ejaculation in
90% of patients.
10% of patient you can't preserve ejaculation even with modified RPLND.
25% of patients have LNs involvement at time of diagnosis so only 25% of
testicular cancer patients need RPLND.
the remaining 75% of patient we do what's known as active surveillance; which means
not to expose patients to the risk of RPLND and rather follow them up carefully.
are specific candidates for active surveillance, I am not sure if you need to know
them for the sake of the exam but I don't think so, you can ask the Dr if they are required
from you or not and you'll find them anywhere in the net.

-119-
-120-
 UTI
• Inflammation of the urothelium due to microorganism invasion
• Divided into
1- Upper UTI: pyelonephritis
2- Lower UTI : cystitis ,urethritis, prostatitis
• Most common cause in all is E.coli except in urethritis
• Routes of infection :ascending (m.c )1 hematogenous, lymphatics
• Recurrent UTI : more than 2 infections in 6 months or 3 infections in 1 year
• Isolated UTI : more than 6 months between one infection and another
• Defense mechanisms that prevent UTI: lysozymes, lactoferrin, IGA in urine ,flushing
effect of urine, low urine PH and high osmolarity, mucopolysaccaride coating of the
bladder
• Factors increase bacterial virulence : adhesion factors, capsule, toxins, enzymes

o Uncomplicated UTI : UTI in structurally and functionally (both) normal urinary tract
with normal immunity and low risk of bacterial virulence ,majority are females
o Complicated UTI : one of these or more present; male, pt with structurally or
functionally abnormal kidney , immunocompromised , chance of increased bacterial
resistant (hx of ABx use or hospitalization) , majority are males i.e if UTI occurred in a
male its most likely to be complicated

1. Pyelonephritis :

• It means infection of the renal parenchyma and renal pelvis

• Risk factors : VUR, OM, pregnancy, congenital malformation , indwelling
catheter
• Acute pyelonephritis :

• Presentation ranges from mild illness to sepsis, pt may be well or ill

• Symptoms and signs : loin pain, nausea, vomiting, fever, chills, rigor , may be
associated with lower UTI symptoms, tachycardia , costovertebral angle
tenderness
• It's a clinical diagnosis but you should rely on evidence of infection by doing
urine analysis and culture 1 also do CBC where leukocytosis may dbe found ,
KFT (creatinine ,BUN )
Blood culture is preserved for immunocompromised patients
• Treatment :
1) Outpatient treatment with oral antibiotics: used in patients with mild
uncomplicated pyelonephritis and are systematically well, antibiotics
used usually are flouroquinolones 1 others are broad spectrum

-121-
 penicillins ( ampicillin , amoxicillin ) , cephalosporins , trimethoprem-
sulfamethoxazole
2) In patient treatment with IV antibiotics indications:
Extremes of age
Complicated infection
Persistent vomiting where pt cant tolerate oral intake and oral ABx
Failure of outpatient treatment

Treatment is with IV flouroquinolones , aminoglycoside with/without

ampicillin or third generation cephalosporin for 7-14 days

Urine culture should be repeated one- two weeks after

completion of antibiotics

Case #1 : 35 year old male medically free, presented to ER with right flank pain of two days
duration associated with fever, chills, rigor and lower urinary tract symptoms patint looks ill ,
temp= 39.5 orally ,HR= 120 beats/m in regular , BP=120\80 , RR= 20\min abd<:>men was soft lax
with right renal angle tenderness, invx showed leukocytosis elevated creatinine, UA showed
bacterial growth .

OX: it's a complicated UTI until proven otherwise (cus he is a male) , note that complicated UTI
is an indication for imaging to look for anatomical abnormalities or stone and the best modality
is non contrasted CT scan

If stone is found then its an obstructive pyelonephritis which is

a life threatening condition where pt may became shocked at
anytime so Management will be with IV fluids , IV antibiotics
send blood culture don't remove the stone at this time but it's
a must to relieve the obstruction by putting a uretric (double j)
stent pr a nephrostomy tube , after pt stabilization manage to
remove t he stone

Case #2 : a 70 yaer old female, diabetic, with IHO came with bilateral flank pain ,fever, lower
UTI symptoms , +ve renal angle and suprapubic tenderness .

OX : complicated UTI cus she is diadetic with abnormal kidney function and she is
immunocompromised , imaging is needed

U\A

o It includes macroscopic appearance of urine , dipstick , microscopic

o Bacteruria : presence of significant amount of bacteria in urine> 10"5 \ml, it may be
symptomatic or asymptomatic, asymptomatic bacteruria should be treated in pregnant
, children , immunocompromised
o Pyuria : presence of significant WBCs in urine>= 5cells \HPF
o sterile pyuria : presence of WBCs without bacteruria , occurs in cases of incomplete ttt of
UTI , CIS , urolithiasis , TB and clamydial infx
o hematuria : presence of significant amount of RBC in urine >=3 cells \HPF

-122-
 • Emphysematous pyelonephritis : it's a severe form of acute pyelonephritis caused by a
gas forming bacteria such as E.coli, klebsiella , proteus, occurs in diabetics and pts
with obstruction , it carries a high mortality

• Xanthogranulomatus pyelonephritis : severe infection ass with renal calculi and

obstruction , caused by E.coli and proteus, U/s shows enlarged kidney with echogenic
material, CT scan shows renal calcification difficult to differentiate from CA

• Chronic pyelonephritis :fibrosis due to recurrent or persistent infection, occur in VUR

pts, mstly in upper and lower poles of the kidney , presentation is asymptomatic or
with renal failure

2. Cystits:
• May be infectious and non infectious
• Types:
-acute infectious
-cystitis cystica and glandular cystitis
-follicular cystitis
- hemmorhagic
-interstitial

• Acute infectious cystitis : symptoms are irritative dysuria, urgency 1 offensive

smelled urine 1 hematuria , suprapubic tenderness with or without fever

Case #3: 30 yo newly married female presented with dysuria , frequency, urgency, no loin pain
, no fever, abdominal exam is free apart from suprapubic tenderness

DX: honey moon cystitis ( due to trauma to genital area ) , invx : in this case specifically you can
start ttt without doing UA or culture , Mgt : rea ssurance , PO ABx trimethoprem -
sulfamethoxazole

3. Urethritis :
• Symptoms: dysuria, discharge , meatal and penile shaft pain, but no irritative
Symptoms
• MCC is neisseria gonorrhea (gram -ve diplococci)
• Divided into
gonococcal : present with sudden onset of large amount of yellow
discharge and mild dysuria
non gonococcal : caused by clamydia trachomatis , present with
gradual onset of clear discharge
• DX is by culture from urethral swab
• Ttt: for N.gonorrhea sefoloxime, for C.trachomatis azithromycine

=> if Dysuria without frequency then its urethritis

-1 23 -
 4. Prostatitis :
• 5% prevalence
• Due to reflux of infected urine into prostatic duct
• Risk factors : UTI, urethral catheter
• Ecoli, proteus, klebsiella
• Classification :
Acute bacterial prostatitis
Chronic bacterial
Chronic pelvic pain syndrome
Asymptomatic inflammatory prostatitis (histologic)
o Acute prostatitis : presentation is with lower urinary tract symptoms in
the absence of loin pain and presence of fever (most imp distinguishing
factor), ttt is with broad spectrum ABx, it requires hospitalization,
avoidance of urethral catheter, if needed use suprapubic catheter
o Chronic prostatitis :treatment is with NSAID, steroids, alpha blockers,
Salpha reductase inhibitors, microwave heat therapy if refractory to
medical ttt

Notes :

o Bacteria without WBC and without Sx: colonization

o Bacteria and WBC without Sx : asymptomatic bacteruria
o WBC without bacteria : sterile pyuria
o Relapse is with the same strain
o Reinfection is with different bacteria
o Nocturia : if pt awaked > 2times at night to void
o Upper urinary tract drainage is by double J stentor nephrostomy, while lower urinary
tract drainage is by urethral or suprapubic catheter

Zaina almusa

- 124-
 Infertility

Infertility in 30% of the cases is due to male causes, and in it we are

concerned with testicular function and sperm conducting system.
Spermatogenesis happens in seminefrous tubules

2n "Spermatogonia" (is on basement membrane, it is the source of

seminoma and teratoma) -7 4 sperms ln each in the lumen -7
conducted via microscopic sperm conducting system (seminefrous
tubules and vasa efferentia) -7 macroscopic conducting system

LH acts on interstitial cells (Leydig) to secrete testosterone, FSH acts on

seminefrous tubules to promote spermatogenesis and secrete inhibin
that suppresses FSH secretion controlling it within normal range; in
testicular failure inhibin is reduced and FSH increases indicating
testicular failure.

The 2 layers of tunica vaginal is are a part of peritoneum lying anterior

to testes (since it is a peritoneal organ in its emberyological origin) so if
there is a painless swelling anterior or engulfing the testes and it
transilluminates suspect hydrocele.

Vasa efferentia will unite to form one convoluted tubule -7 epidydimis

which is composed of head, body and tale then the tail straightens
forming the vas deferens that will ascend until reaching posterior to the
bladder where it forms a pouch (seminal vesicle), and seminal vesicle+

-125-
vas deferens give ejaculatory duct which opens in the prostatic urethra
near the vero montana near the apex of the prostate.

Blockage can take place at any level causing Azospermia:

l)vasa efferentia: this leads to spermatocele that is on the upper pole

of the testicle posteriorly and is treated by careful surgical excision.

2)epidydemis and vas deferens: due to inflammation secondary to

infection by Chlamydia, Gonorrhea, Granulamatous infections as TB. If
the site of blockage is at the beginning of the vas or at the end of the
tail of the epidydemis we can see congestion of epidydemis by
transrectal U/S

Ttt: if at tail of epidydemis we anastomose body of epidydimis to vas

deferens (epidydimovasostomy)

It at the vas deferens localize site of obstruction by intraoperative X-

ray (vasography) and we do vasovasostomy

If at vero montana resection of vero montana

** Non-obstructive causes of infertility:

!)varicocele: treated by inguinal ligation.

2)Cryptorchidism: dysplastic testicle

3}0rchitis: caused by mumps

4) trauma

-126-
* If a patient is azospermic but with normal hormonal profile and no
congestion of seminal vesicles or epidydimis 7 we extract sperms
intraoperatively (try from epidydimis and if failed try from testicles and
if failed open testicles and take a tissue specimen and then by
centrifugation we extract sperms, those are called sperm retrieval
techniques.

The End
Done by Amr Ghazzal

-127-
-128-
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-130-
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-131-
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pn..cl-nisone- -+
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[ 'Sfr<>limu..-5 A:zeJlliofdne or cyctosf>on'rl ]

-132-
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- 133-
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- 134-
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-135-
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in !:he csperma.l::fc eorJ.
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5
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• (<tO"/.) oJ VDJ,'Coc.-de on LL C:Stde 7 due... ;::l;o- :

rf ll. inl:eri'IA.i. spu mcJ::;;c v. (RL(.nJ f?.t.siae)
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·

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-136-
,.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .: 6

Urology notes for OSCE:

Finasteride (proscar)
Type IT 5 - a reductase inhibitor

Medical uses :
1. Hair loss. 2.BPH.

Side effects:
1. Gynecomastia. 4.. Impotence.

2. Prostate cancer. 5 .. Low ejaculation volume.

3. Breast cancer. 6. Erectile dysfunction.

5- a reductase inhibitors:
1. Type I (active in liver, non-genital skin, some areas
in the brain).

2. Type II (in the tests).

- In PR examination for prostate: each finger width=20 gm.

- Urethral strictures :

the bulbar urethra (mostly)

1. Traumatic (traumatic cystogram, Foley's, TURP, TURT).

2. Tumor. 3. Congenital.
4. Infection (Urethritis due to gonoccocal infection).
*Keep in mind :

(once there is a stricture, the patient never becomes cured, there is always a recurrence).

-137-
,..........................................................
Xatral:
.
Al fazosin, selective short acting a. - blocker.

1. Prostate capsule relaxation. 2. Bladder neck relaxation.

Also we can give it for uretral stones, causes dilation in the lower ureter.

-?Side effects:

to remember it we know that in every patient with prostate problem, we should do PR

examination SOOOOO, all patients

HADPR
H: Headache.

A: Asthesia (general weakness).

D : Dizziness.

P: Postural hypotension.

R: Retrograde ejaculation (8%), most C?mmon

Q :Can we give a female pt (Xatral) with BOO, and why???

Yes, because the neck of bladder has an a.- receptor, not only in the prostate.

- KUB differs from normal x-ray by:

1. Higher penetration.

2. Needs bowl preparation.

3. Exposure.

-138-
............................................................
**Triad of pylonephritis:

1. Febrile pt. 2. Loin pain. 3. +ve urine analysis.

- Complete obstruction, needs 6 weeks to cause irreversible damage usually.

- US, sensitive to renal stones but not sensitive to uretric stones.

+ve costovertebral angle tenderness D.Dx:

1. Pylonephritis. 2. Stones

- Varicocele :
abnormal dilated testicular veins (pampiniform plexus).

7 classification:

Clinical:

1. Grade I (small): palpable with valsalva maneuver only.

2. Grade II (medium): palpable without valsalva.

3. Grade lli (large): visible.

(always examine your patient on standing position).

-US:

2-2.5 mm grade I.

2.5 - 3 mm grade II.

> 3 mm grade Ill

-139-
,.
........................................................... s
More common on the left side due to :

I. perpendicular insertion of the left testicular vein into high pressure system (right into low
pressure system).

2. reflux of adrenal metabolites (high cortisol).

veins ligation during varicocele surgery we don't

ligate peri-vasal vein due to risk of injury to the vas.

7 Best procedure is (microscopic inguinal ligation).

-prostate cancer:
If advanced just hormonal therapy+ treatment of the symptoms (palliative therapy).

I)rugs for PCA treatment:

I. Casodex: anti- androgen/ PO.

2. Zoradex: LHRH agonist

Zoradex is given in continuous way thus its effect is also continuous and this will end up by
the suppression due to non Pulsatile sex hormone production.

- Zometa (IV Injection), once monthly: zoledronic acid.

We should give it in patients with prostate cancer treated with androgen deprivation therapy
to prevent skeletal fracture.

***keep in mind that prostate cancer can induce bone mets, so always check
Ca++ level ·a nd do bone scan to detect any bone resorption.***
- detrusitol: anti cholinergic drug, for Neurogenic bladder (urgency).

- DMSA: to see cortex.

- Eiaculation:

* volume: 2-8 ml now 1 ml.

* number: 20 x 106 /ml or 40 x 106 /ejaculation.

* motility > 50% now >40% anterograde movement.

*morphology> 30% now> 15% fuut dr. Samer al Rawashda said it's >4%.1

••
-140-
 •

............................................................
**Bladder cancer: **
Presentation: Intermittent painless grass hematuria.

1. Superficial < T2 TURT.

2. Muscle invasive : radical cystectomy.

3. with mets: radio and chemotherapy.

?Follow up :

1.Urine cytology (not used here).

2.Check cystoscopy

(every 3 months I for 2 years . ... then ... Every 6 months for 1-2 years ... then 1/Q year).

3 .Anytime if there is regrowth it's back to cystoscopy every 3 months

More common in males , 3 : I

Risk factors:

1. Smoking (most common).

2.Age.

3. Exposure to aromatic hydrocarbons.

read TNM classification in ( dossya © )

1. obstructive symptom due to presence of residual urine.

2. irritative symptom due to initation of the bladder wall

-141-
,.
........................................................... .
- Foley's catheter elevates PSA for 2-3 days.

- types ofprostatic biopsy:

l. trans-urethral.

2. per-rectal (most common).

3. perianal.
- risk of septicemia/ so to avoid this in JUH,

we give (IV-antibiotic pre- op, then oral antibiotic for 1 week).

-Cystitis (doesn't lead to systemic symptoms because it is an open system).

- prostatistis : is lower UTI, causes systemic symptoms

(patient is febrile + other symptoms of LUTI).

-Symptoms:

1. Painful erection.

2. Painful ejaculation.

3. dysuria during ejaculation.

4. peri-anal pain.

-spermatocele (dead sperms):

Doesn't transulimnate, usually no needfor treatment especially in :

1. young.

2. male concerningfertility.

'

-142-
...............................................................
,..
**bladder stones:

-?most common in infective (struvite),

-?most common in non-infective (uric acid).

- emergency cases in urology:

1. torsion. 3. acute retention.

2. priapism. 4. trauma

- In cystoscopy we use glycine not saline, why????

Because it is a hypoasmolar solution and doesn't contain (Na

so will not transmit electrical current. But it can cause TUR
·· syndrome (low K+, low Na+, visual disturbances {because
glycine is a neurotransmitter in the retina}, and finally
Bradycardia).

-PSA (Important in OSCE) :

+ PSA (Prostate specific antigen).

+ ·causes of:

+ High PSA: (infection PBH, malignancy, trauma, prostate manipulation CPR, Foley's).
Low PSA: (Prostatectomy, drugs {Finasteride})

+ PSA half life (normal 2- 3 days).

+ Total PSA:
< 4 (normal).

4-10 (calculate ratio (freeitotal) if< 18% malignancy).

> 10 (malignancy).

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................................................................
"' Erectile Dysfunction :
+ There is a connection between 2 - corpus cavemosum so in treatment (intraurethral
injection we inject in one side only).

• But there is no connection between corpus cavernosum and the glans penis.

• Relaxation of corpus cavemosum = erection.

+ Ereetile Dysfunction due to vascular causes usually precedes coronary symptoms by 2 - 3

days (because it effects on penile as which is narrow and multiple ).

-In intraurethral injection we use: (3 Ps)

l.PGE.
2. Papaverine.

3. Phentolamine.

-Benefits ofViagra in patient with erectile dysfunction from DM is-56 %.

- Causes of erectile dysfunction (Important in OSCE) :

IMPOTENCE
I : Inflammation ex prostatitis.

M: Mechanical ex peyronies Disease.

P: Psychological ex (anxiety, stress, lack of attract).

0 : Occlusive (Vascular).

+ Arteriogenic (HTN, smoking, DM CPVD).

+ V asogenic.

T: Trawna ex (pelvic fracture, penile trauma, spinal cord injury).

E : Extra factors ex (Iatrogenic, post surgery, high age, cirrhosis).

-
•
-144-
,
.............................................................

N: Neurogenic ex (MS, Parkinson, spina bifida ......... ).

C: Chemical (drugs), examples of chemical drugs:

1. antihypertensive (b-blocker, thiazide, ACEI).

2. anti arrhythmic (amiodarone).

3. anti androgen (proscar).

4. anxyolytics (benzodiazepine) . ..... ..................... etc

E : Endocrine (DM, hyperprolactinaemia, hypogonadism).

**Erection: Para- sympathetic.

**Ejaculation : Sympathetic.

Emission Vs Ejaculation.

I )Emission (closure of internal sphincter and production of seminal

vesicle and prostatic secretions).

2)Ejaculation (Rythrnetic contraction

-In Neurogenic bladder:

1. What is the treatment????

7 Andcho/inegic.
2. Mention one????
7 Oxybutanin.

- capacity of bladder in :

1. adults: 500 mi. 2. children : ( (age+ 2) x 30 ).

-pons (responsible for coordination between sphincter and detrusor M).

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.............................................................. .

- OSCE: Ciprojloxacin.
• it is antibiotic of the fluroquinolone drug class.

• 2nd generation.

• its function is through the (DNA- gyrase inhibitor).

• medical use:
1. chronic bacterial prostatitis.

2. UTI.

3. Acute uncomplicated cystitis in females.

4. Lower respiratory tract infections.

5. Acute sinusitis.

6. Bone+ skin +joint infection.

• contraindicated in :
I. pregnancy due to (risk of spontaneous abortions and birth defects).

2. pediatric age patients due to (effects growth).

+ Side effects:
I. irreversible peripheral neuropathy.

2. tendon damage.

3. heart problems (prolonged QT interval also torsades de point).

4. pseudo membranous colitis.

5. Rhabdomyolysis.

6. Steven's Jonson syndrome.

'.
••
-146-
..........................................................
-Renal trauma :
-gold standard is (triphasic CT-scan) then followed by KUB.

- Indications of CT-scan in :

1. gross hematuria.

2. microscopic hematuria+ Urodynamic instability.

3. acceleration- deceleration injury.

4. penetrating injury.

5. presence of other organ's injury.

Most cases are treated by (conservative treatment):

l. complete bed rest.

2. continuous vital sign /Q 1.

3. CBC twice/day.

4. CT once/day.

5. IV-fluid.

6. IV blood.

(IV-fluid and IV-blood only if needed).

Types ofsurgery:

1. reno-raphy (in stable patient) organ sparing.

2. nephrectomy : in unstable patient.

- retropupic space= space ofrezius.

- JJ-insertion (cause perforation sometimes but also it is a mode of treatment in other times).

"

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,...........................................................
**hydronephrosis (due to obstruction by:

{stones, clots, fibrosis}.

**For enurisis:

-) Tratement (minirine) which is an anti dirutic honnone, (ADH antagonist).

** D.Dx of orchalgia:
1. idiopathic. 3. epididymoorchitis.
4. trauma
2. nerve entrapment.
-Stones:
< 4 mm: 90% (spontaneously resolved).
4-6 mm: 30% (spontaneously revolved).
> 6 mm : surgery.

-penile fracture :
1. very painfUl (top emergency).

2. rupture oftunica albogenia.

3. symptoms depend on hematoma.
4. Important to focus on sexual Hx.

Black -white -black-white rule in urology©

Tumors more common in :

Black : kidney.

White: bladder.

Black: prostate.

White: testis

-148-
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with my best wishes
BayanAl-Khdour
Especial thax to Ndia Abu-thaimer
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-149-
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